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Sympathomimetic amines의 혈당 상승작용에 대한 재검토

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 Studies on the hyperglycemic activities of sympathomimetic amines 
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[영문] Among the variety of metabolic effects attributed to the catecholamines, hyperglycemia has received the most emphasis. The increase in blood suger has been shown to be caused mainly by the stimulation of glycogenolysis in liver and muscle, as a consequence of the activation of phosphorylase (Sutherland and Cori, 1951). However, the precise nature of the adrenergic receptor concerning glycogenolysis in liver has not been clearly demonstrated. There are many publications which indicate that a variety of adrenergic blocking agents will modify the glycogenolytic response to epinephrine. Nickerson(1949) reported that epinephrine-induced hyperglycemia could be completely prevented by dibenamine and there is also in vitro evidence that dibenamine can supress liver glycogenolysis (Craig and Mendell, 1959.) On the other hand, Ellis et al. (1957) reported that dibenamine could not block the epinephrineindueed hyperglycemia in the intact cat and according to Havel and Goldfien(1959), dibenamine is said to block free fatty acid mobilization but not hyperglycemia in the dog. More recently, Mayer et al.(1961) demonstrated that dichloroisoproterenol(DCI) almost completely abolished the increase in blood glucose produced by epinephrine and norepinephrine, while phenoxybenzamine failed to block this. From the above studies, analyzing the mechanism of the epinephrine hyperglycemia by utilizing adrenergic blocking agents, it is not possible to establish definitely the character of the adrenergic receptor concerning glycogenolysis in liver. The present experiment was undertaken to clarify the nature of the receptor on the basis of Ahlquist's classification of the adrenergic receptors. Recently, some of the sympathomimetic amines such as tyramine, ephedrine and phenylethylamine, etc., have been shown to exert their cardio-stimulant action by releasing catecholamines in the heart. It was decided also to examine whether this is true for the hyperglycemic response to ephedrine. Healthy albino rabbits weighing approximately 2.0kg of body weight were employed in this experiment. Blood samples were withdrawn from the ear vein at various time intervals after the administration of drugs and glucose was determined in duplicate according to the method of Folin-Wu. Results and Discussion 1. The intravenous administration of epinephrine 10.0㎍/kg produced a sudden rise in the concentration of blood sugar, resulting in the maximum value within 15 minutes. The maximal increase of blood sugar was about 40 per cent of the control value. This hyperglycemia gradually returned to the normal level, but not completely within 2 hours. 2. The intravenous administration of norepinephrine 10.0㎍/kg produced a hyperglycemia but the increase in blood sugar was only 10% of the control value. A large dose(50.0㎍/kg) of this drug produced about 30% increase in blood sugar over the normal value. From this result, the hyperglycemic activity of epinephrine is about 5 times as great as that of norepinephrine. 3. Dichloroisoproterenol(DCI) which specifically blocks the adrenergic β-receptor, produced a transitory hyperglycemia soon after the administration. When the rise in blood sugar had returned to the normal level, the intravenous injection of epinephrine(10.0㎍/kg) increased blood sugar, but this was markedly less than that observed in normal rabbits. Although larger doses of DCI inhibited still more the epinephrine-induced hyperglycemia, they failed to inhibit it completely. 4. Dibenzyline, which is a blocking agent of adrenergic α-receptors, inhibited markedly but not completely the hyperglycemia induced by epinephrine. 5. Pretreatment with DCI and dibenzyline inhibited completely the hyperglycemia by epinephrine. 6. Dihydroergotamine (DHE), which is known to block both adrenrgic α-and β-receptors, also inhibited completely the hyperglycemia produced by epinephrine. 7. A study of various doses of ephedrine on the blood sugar of rabbits showed that doses of 25mg/kg or more resulted in a profound longlasting hyperglycemia. 8. The intraperitoneal injection of reserpine (10.0mg/kg) in rabbits markedly reduced the catecholamines in the liver. These reserpine-treated rabbits exhibited no hyperglycemic response to ephedrine but responded to epinephrine as did normal rabbits. 9. After pretreatment with bretylium, which blocks the release of catecholamines from their deports, ephedrine (25.0mg/kg) failed to produce its hyperglycemic activity, but epinephrine produced a marked rise in blood sugar as usual. From the above results, there exist in the liver both the adrenergic α-and β-receptors proposed by Ahlquist(1948). Epinephrine produces hyperglycemia by acting on both receptors. The studies concerning the mechanism of the hyperglycemia prpduced by ephedrine suggest that ephedrine causes arise in blood sugar indirectly by releasing catecholamines, especially norepinephrine, in the body.
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2. Thesis / Dissertation (학위논문) > 1. College of Medicine (의과대학) > Ph.D. (박사)
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